Phillips N E, Campbell P A
J Immunol. 1981 Aug;127(2):495-500.
CBA/N mice have an X-linked immunodeficiency that includes a deficient humoral response to sheep red blood cells (SRBC). In order to study the cellular mechanisms of this deficiency we have examined helper T cell function to SRBC in an adoptive transfer system by using 2 different sources of helper T cells. When thymocytes were used as the source of helper T cell precursors in an adoptive transfer system, CBA/N thymocytes were as effective as CBA/Ca thymocytes in inducing CBA/Ca bone marrow cells to develop into both direct and indirect anti-SRBC plaque-forming cells (PFC). However, when SRBC-primed, irradiated recipient mice were used as the source of helper T cells, primed and irradiated CBA/N recipients developed significantly fewer direct and indirect anti-SRBC PFC than similarly treated CBA/Ca recipients when reconstituted with CBA/Ca bone marrow cells and challenged with SRBC. This difference in radioresistant helper T cell function was also observed when primed, irradiated (CBA/N X DBA/2)F1 defective male and nondefective female mice were used as recipients of F1 female bone marrow cells and SRBC, confirming that this defect is a part of the X-linked CBA/N immunodeficiency. This deficiency in radioresistant helper T cell function in CBA/N mice does not appear to be due either to suppressor T cell function, or to a negative effect of the CBA/N environment on either B cell maturation, T cell-B cell cooperation, or helper T cell function. We conclude that antigen-primed helper T cell function in CBA/N mice is radiosensitive. Possible reasons for this are evaluated and discussed.
CBA/N小鼠存在X连锁免疫缺陷，包括对绵羊红细胞（SRBC）的体液免疫反应缺陷。为了研究这种缺陷的细胞机制，我们在过继转移系统中使用两种不同来源的辅助性T细胞，检测了针对SRBC的辅助性T细胞功能。当过继转移系统中使用胸腺细胞作为辅助性T细胞前体的来源时，CBA/N胸腺细胞在诱导CBA/Ca骨髓细胞发育为直接和间接抗SRBC斑块形成细胞（PFC）方面与CBA/Ca胸腺细胞一样有效。然而，当用经SRBC致敏、照射的受体小鼠作为辅助性T细胞的来源时，在用CBA/Ca骨髓细胞重建并用SRBC攻击后，经致敏和照射的CBA/N受体产生的直接和间接抗SRBC PFC明显少于同样处理的CBA/Ca受体。当用经致敏、照射的（CBA/N×DBA/2）F1缺陷雄性和无缺陷雌性小鼠作为F1雌性骨髓细胞和SRBC的受体时，也观察到了这种抗辐射辅助性T细胞功能的差异，证实这种缺陷是X连锁CBA/N免疫缺陷的一部分。CBA/N小鼠抗辐射辅助性T细胞功能的这种缺陷似乎既不是由于抑制性T细胞功能，也不是由于CBA/N环境对B细胞成熟、T细胞 - B细胞协作或辅助性T细胞功能的负面影响。我们得出结论，CBA/N小鼠中抗原致敏的辅助性T细胞功能对辐射敏感。对此可能的原因进行了评估和讨论。
